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PubMed1995

Atrial natriuretic peptide release at rest and with exercise after cardiac transplantation with bicaval anastomoses.

Bicaval anastomoses in orthotopic cardiac transplantation offer the advantage of preserving the right atrial geometry. To elucidate the impact of this anastomotic technique on atrial natriuretic peptide plasma levels at rest and with exercise, nine patients were submitted to a symptom-limited supine exercise test. Atrial natriuretic peptide plasma levels in samples obtained from the right atrium were elevated at rest (274.4 +/- 60.4 pg/ml), at peak exercise (438.1 +/- 71.7 pg/ml), and thereafter (328.1 +/- 71.2 pg/ml) with respect to normal reference values of 21 +/- 1 pg/ml at rest and 92 +/- 14 at peak exercise. Renin, angiotensin, and aldosterone plasma levels were almost normal and did not indicate any pathologic processes in volume homeoostasis. Right-sided hemodynamic parameters were not correlated with atrial natriuretic peptide secretion. An adverse relationship between cold ischemic time of the donor organ and atrial natriuretic peptide release was found (r = 0.88, p < 0.0008), indicating that endocrine cardiocytes are sensitive to prolonged ischemia. Atrial natriuretic peptide release may thus be independent of the surgical approach, and other unique characteristics of the transplanted heart, such as denervation, are more likely to be responsible for elevated atrial natriuretic peptide plasma concentrations after orthotopic heart transplantation.

Adult↗

PubMed1995

Atrial pressure and experimental atrial fibrillation.

A possible profibrillatory effect on the atria of an elevated atrial pressure and the site of atrial stimulation was examined. In 15 anesthetized dogs, right or left atrial or biatrial pacing was applied at a high rate (300-600/min) for 5 seconds at double threshold intensity under a wide range of atrial pressures achieved by venous or arterial transfusion or bleeding. Induction of atrial fibrillation in 236 of 1,971 pacing runs was associated with a significantly higher (P < 0.001) atrial pressure (21.6 +/- 12.2 mmHg, mean +/- SD) than maintenance of sinus rhythm (16.8 +/- 11.1 mmHg in 1,735 of 1,971 pacing runs). Stimulation of the right atrium resulted in atrial fibrillation more frequently than left atrial or biatrial stimulation, with biatrial stimulation less frequent than right or left atrial stimulation. The induction of atrial fibrillation was related to the atrial pressure and to the site of stimulation but not to the pacing rate or the prepacing heart rate. The prepacing heart rate, associated with failure to induce sustained atrial fibrillation, was higher than that associated with atrial fibrillation in 12 of 15 experiments (significantly in 6) and not significantly lower in 3 of 15. Atrial fibrillation lasting 1 minute or more was more frequently associated with simultaneous stimulation of both atria than of either atrium alone. Thus, an elevated atrial pressure may facilitate the induction of atrial fibrillation. The site of stimulation also plays an important role for both the induction and maintenance of atrial fibrillation in this model.

Animals↗

PubMed1991

Human atrial natriuretic factor and renin-aldosterone in paracetamol induced fulminant hepatic failure.

It has been postulated that deficiency of a putative natriuretic factor, or resistance to such a factor, may contribute to sodium retention in fulminant hepatic failure. Levels of plasma human atrial natriuretic factor (h-ANF), plasma renin activity, and aldosterone concentration were measured in 33 patients with fulminant hepatic failure due to paracetamol overdose, and 12 healthy control subjects. Levels of h-ANF were raised only in patients with evidence of severe renal impairment (serum creatinine greater than 300 mumol/l and urine output less than 100 ml/24 hours). h-ANF values were median 4.15, range 2-9 pmol/l and 10.1, 1-25 pmol/l for the control and severe renal impairment groups respectively (p less than 0.001). In the latter plasma renin activity was raised compared to that in control subjects (median 19.8, range 1.04-41.7 and 2.86, 1.87-5.9 pmol/l/h respectively, p less than 0.02). Plasma aldosterone concentration was also raised in patients (2176, 199-6894 pmol/l compared to 368, 133-578 pmol/l in control subjects, p less than 0.01). Haemodialysis induced changes in circulating h-ANF which correlated with volume and right atrial pressure changes (p less than 0.001 and p less than 0.05 respectively). In six patients with no or mild renal failure infusion of 900 ml 5% human albumin solution caused a significant increase in plasma h-ANF (p less than 0.05) without natriuresis or diuresis, a finding compatible with the hypothesis that there may be resistance to h-ANF in this group. The present findings indicate that there is no deficiency of h-ANF in fulminant hepatic failure and that known mechanisms of h-ANF release are not impaired.

Acetaminophen↗

PubMed1998

Chronic infusions of brain natriuretic peptide in conscious sheep: bioactivity at low physiological levels.

1. The circulating cardiac hormones atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) have similar bioactivity, as judged by comparative short-term studies. However, no study has reported the effects of longer-term administration of BNP. Accordingly, we have compared the haemodynamic, hormonal and renal actions of chronic (4-day) administration of BNP and ANP (0.5 pmol. min-1.kg-1) in a vehicle-controlled study in normal conscious sheep. 2.BNP infusions raised plasma BNP levels within the physiological range (4 pmol/l increment, P<0.001) and increased cyclic GMP levels (P=0.01). BNP infusions induced significant falls in right atrial pressure (P=0.048), stroke volume (P=0.014) and cardiac output (P=0. 003) associated with a rise in haematocrit (P=0.001). There were no significant renal effects or changes in renin-aldosterone. By comparison, equimolar infusion of ANP induced a smaller increment in plasma ANP levels (2 pmol/l, P=0.03) with qualitatively similar but statistically non-significant changes in plasma cyclic GMP and haemodynamic indices.3.In conclusion, chronic low-dose infusions of BNP elevate plasma cyclic GMP levels and induce significant haemodynamic actions. This study provides evidence that subtle variations in circulating BNP levels, well within the physiological range, may be important in long-term cardiovascular control.

Analysis of Variance↗

PubMed1997

Combined inhibition of endothelin and angiotensin II receptors blocks volume load-induced cardiac hormone release.

Volume expansion has been shown to increase plasma atrial natriuretic peptide (ANP) levels, but the precise role of paracrine and autocrine factors in stretch-induced cardiac hormone release is not clear. In the present study, we report the effects of endothelin (ET) and angiotensin receptor (AT receptor) antagonists on baseline and atrial stretch-induced immunoreactive ANP (IR-ANP) and immunoreactive N-terminal ANP (IR-NT-ANP) release in vivo by using BQ-123 (ETA receptor antagonist), bosentan (ETA and ETB receptor antagonist), and losartan (AT1 receptor antagonist). Intravenous administration of BQ-123 had no significant effect on baseline hemodynamics in conscious rats, whereas bosentan (10 mg/kg) and losartan (10 mg/kg) decreased slightly (4 to 7 mm Hg, P < .05 to .001) the mean arterial pressure. Both the ETA receptor antagonist BQ-123 and ETA/ETB receptor antagonist bosentan decreased plasma ANP and NT-ANP responses to volume load (P < .05 to .001), whereas the AT1 receptor antagonist losartan had no significant effect on this response. The relative increase in plasma IR-ANP corresponding to a 3 mm Hg increase in right atrial pressure was 2.7-fold in the vehicle-treated group. BQ-123 (0.3 and 1.0 mg/kg) decreased this response 2.5- and 2.1-fold (P < .05); bosentan (3 and 10 mg/kg), 1.7-fold (P < .001) and 1.9-fold (P < .05); and bosentan (10 mg/kg)+losartan (10 mg/kg), 1.6-fold (P < .001). The responses in plasma IR-NT-ANP decreased simultaneously. These results indicate that combined inhibition of ETA/B and AT1 receptors almost completely blocks ANP response to acute volume load. Therefore, our study shows that endogenous paracrine and/or autocrine factors liberated in response to atrial wall stretch rather than myocyte stretch itself are responsible for the activation of ANP peptide secretion in response to acute volume load. Our results also show that ETA receptors are more important in the regulation of mechanical stretch-induced changes in cardiac hormone secretion than AT1 receptors.

Angiotensin II↗

PubMed1995

Changes in atrial natriuretic peptide and plasma renin activity following changes in right atrial pressure in patients with chronic renal failure.

Since it was first discovered in the early 1980s, the role of atrial natriuretic peptide (ANP) in the control of fluid and electrolyte balance and blood pressure has been extensively studied in both health and disease. We report here a study of ANP and its relationship to corresponding changes in right atrial pressure (RAP) in patients with chronic renal failure (CRF) on haemodialysis compared to healthy controls. Although there was a positive correlation between RAP and ANP in both groups, the changes in ANP following changes in RAP between the two groups were not statistically significant. A unique observation was the response of RAP to changes in posture, with RAP falling significantly as expected in healthy controls in contrast to the exceptional absence of a significant fall in patients with CRF. Healthy controls demonstrated appropriate postural changes in plasma renin activity (PRA) despite marked suppression of PRA levels due to salt loading, in complete contrast to patients with CRF who, despite chronic fluid overload and elevated levels of ANP, continued to have grossly elevated PRA levels that failed to change significantly in response to changes in posture.

Atrial Function, Right↗

PubMed1991

Atrial natriuretic peptide responses during anaesthesia in patients with refractory cardiomyopathies.

In patients with congestive heart failure, the release of atrial natriuretic peptide (ANP) is decreased. This study sought to determine the extent of ANP, sympathetic and haemodynamic responses to acutely increased atrial pressure in patients with cardiomyopathies undergoing orthotopic cardiac transplantation. Haemodynamic variables, plasma ANP, norepinephrine, and epinephrine concentrations were measured in 17 patients at five times before and after induction of anaesthesia using either ketamine 1.5 micrograms.kg-1 or sufentanil 3.6 +/- 0.3 micrograms.kg-1. Preinduction values in the ketamine and sufentanil groups were not significantly different. Compared with preinduction values, increases in mean arterial pressure (26%), pulmonary capillary wedge pressure (90%), right atrial pressure (107%), and heart rate (24%) occurred in the ketamine group while cardiac index decreased by 19% (P less than 0.05). Haemodynamic variables in the sufentanil group did not change at any of the times studied. Plasma concentrations of atrial natriuretic peptide were not different within or between treatment groups. Following tracheal intubation plasma norepinephrine levels increased by 116% in the ketamine group (P less than 0.05), but did not change in the sufentanil group. Plasma norepinephrine concentrations differed significantly between the ketamine and sufentanil groups. There were no differences in epinephrine concentrations in either group. Despite the anticipated haemodynamic and catecholamine differences found between the ketamine and sufentanil groups, the levels of plasma ANP were similar. Based upon these results, it is concluded that ANP exerts little influence in the control of fluid volume or blood pressure in patients with refractory cardiomyopathy.

Adult↗

PubMed2002

Divergent effects of ANP and BNP in acute heart failure: evidence for a putative BNP-selective receptor?

OBJECTIVE: Since the pathophysiology of natriuretic peptides in chronic heart failure (HF) is not uniform, we hypothesized that atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) may also have differential effects in acute HF. Our aim was to compare the haemodynamic actions of ANP with BNP, using a classical vasodilator as the control, in greyhound dogs with acute pacing-induced HF. DESIGN AND METHODS: The right ventricles of eight anaesthetized dogs were paced (193 +/- 4 bpm) until pulmonary capillary pressure (PCP) increased to approximately 15 mmHg. In each animal, according to a randomized within-animal design, haemodynamic responses to equimolar (10 pmol/kg per min) infusions of ANP and BNP were compared with those to sodium nitroprusside (SNP). RESULTS: Acute pacing alone increased PCP from 6.6 +/- 0.7 to 15.7 +/- 0.3 mmHg, right atrial pressure (RAP) from 1.9 +/- 0.5 to 4.0 +/- 0.6 mmHg, and systemic vascular resistance (SVR) from 1706 +/- 110 to 2179 +/- 106 dyne s/cm5, and reduced cardiac output (CO) from 4.1 +/- 0.4 to 2.5 +/- 0.2 l/min and arterial pressure from 86.1 +/- 2.4 to 74.5 +/- 2.1 mmHg (all P < 0.01). BNP and SNP improved haemodynamics similarly (CO +13 +/- 3% and +9 +/- 5%; PCP -12 +/- 2% and -12 +/- 2%; RAP -28 +/- 9% and -34 +/- 6%, SVR -15 +/- 3% and -11 +/- 3%, all P < 0.01, except CO with SNP, not significant), but effects of BNP on preload outlasted those of SNP. By contrast, ANP did not improve the haemodynamics. Haematocrit was significantly higher during BNP infusion than with ANP (P < 0.05) or with SNP (P < 0.001). CONCLUSIONS: The haemodynamic responses to exogenous BNP and ANP in acute heart failure were strikingly different. Whereas ANP actions were blunted, BNP response was preserved. Hypothetically, the presence of a putative BNP receptor may explain this finding.

Acute Disease↗

PubMed1994

The acute effects of induced tachycardia on coronary sinus and arterial plasma levels of atrial natriuretic peptide and on arterial catecholamines.

Atrial natriuretic peptide (ANP) was measured in coronary sinus (CS) plasma in seven patients with induced tachycardia. Right atrial pressure (RAP) and femoral artery (FA) levels of ANP, noradrenaline (NA) and adrenaline (A) were measured before and after 5 min with tachycardia. During tachycardia, ANP in CS plasma increased from 381 +/- 273 (mean +/- SD) to 1376 +/- 1191 pmol l-1 (p < 0.0001), and ANP levels in FA plasma from 89 +/- 48 to 231 +/- 151 pmol l-1 (p < 0.005). A significant increase was observed for peak RAP, whereas mean RAP remained unaltered. While no correlation existed between the increase in CS plasma ANP level and RAP, significant correlations were found between the changes in FA plasma ANP and RAP, and between FA plasma levels of ANP and NA. Following tachycardia, significant correlations were found both between ANP in CS and FA plasma and between the changes in these plasma levels. Whereas the changes in FA plasma levels of ANP during tachycardia seems dependent of RAP and arterial plasma levels of NA, the CS plasma ANP level appears to be independent of the two factors, probably because CS plasma ANP are drained mainly from the left side of the heart.

Adult↗

PubMed2001

Electrical conduits within the inferior atrial region exhibit preferential roles in interatrial activation.

Differences between conduction properties of interatrial conduits and their roles in initiation and maintenance of supraventricular arrhythmias remain unclear. Our objective was to determine details of interatrial activation in inferior atrial region and to correlate intra-atrial and interatrial activation patterns with the site of origin of atrial ectopic activation. In 9 dogs, basket-catheters carrying 64 electrodes were deployed into both the right atrium (RA) and left atrium (LA). A 10-electrode catheter was inserted into the coronary sinus (CS). Activation patterns of the RA, LA, and CS were compared during pacing in the CS, in RA inferoparaseptum posterior to Eustachian ridge-tendon of Todaro (TT), and in inferior RA near the CS ostium (anterior to TT). We found that pacing in proximal and middle CS resulted in a RA breakthrough invariably at the CS ostium, consistent with conduction through a CS-RA connection. Meanwhile, LA breakthrough emerged in inferoposterior region (inferior to mitral annulus), suggesting conduction through a CS-LA connection. While pacing in distal CS, LA breakthrough shifted to middle posterolateral wall. Whereas, the RA was activated by the LA directly through the septum. During pacing in RA inferoparaseptum posterior to TT, the LA was activated directly through the septum at 22 +/- 4 ms. Whereas, during pacing anterior to TT, the LA was activated through both the CS and the septum while earliest activation was delayed by 38 +/- 5 ms. In conclusion, both the interatrial septum and CS musculature form electrical conduits in inferior atrial region in canine. Differences in activation properties between the conduits in inferior interatrial region result in selective interatrial activation patterns during ectopic activation.

Animals↗

PubMed1994

Angiotensin and ANP secretion during chronically controlled increments in atrial pressure.

The primary objective of this study was to determine whether angiotensin II (ANG II) has direct effects on the atrium to chronically stimulate the secretion of atrial natriuretic peptide (ANP) by actions that are independent of its vasoconstrictor and fluid-retaining effects that increase ANP secretion indirectly by raising atrial pressure. In five dogs, right atrial pressure (RAP) was controlled at approximately 5.5 mmHg above control levels for 8 days by employing an externally adjustable occluder around the pulmonary artery and a servo-control system, and plasma levels of ANG II were fixed at either normal (days 1-3 and 7-8) or high (days 4-6) physiological concentrations by chronic infusion of captopril+ANG II. When plasma ANG II was maintained at normal levels during servo-control of RAP, plasma ANP concentration increased five- to sixfold and sodium balance was achieved at a reduced arterial pressure (-14 mmHg). In contrast, despite increased plasma levels of ANP, the high rate of ANG II infusion produced marked sodium retention during the initial 24 h; however, the antinatriuresis was not sustained because the servo-control system partially deflated the pulmonary artery occluder to prevent fluid-induced increments in RAP. Moreover, in the absence of a change in RAP, high plasma levels of ANG II did not influence plasma ANP concentration. These findings indicate that the plasma levels of ANP achieved in heart failure increase renal excretory capability and allow fluid balance to be achieved at a substantial fall in mean arterial pressure as long as there is minimal involvement of the renin-angiotensin system.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

PubMed2004

A novel framework of circulatory equilibrium.

A novel framework of circulatory equilibrium was developed by extending Guyton's original concept. In this framework, venous return (CO(V)) for a given stressed volume (V) was characterized by a flat surface as a function of right atrial pressure (P(RA)) and left atrial pressure (P(LA)) as follows: CO(V) = V/W - G(S)P(RA) - G(P)P(LA), where W, G(S), and G(P) denote linear parameters. In seven dogs under total heart bypass, CO(V), P(RA), P(LA), and V were varied to determine the three parameters in each animal with use of multivariate analysis. The coefficient of determination (r(2) = 0.92-0.99) indicated the flatness of the venous return surface. The averaged surface was CO(V) = V/0.129 - 19.61P(RA) - 3.49P(LA). To examine the invariability of the surface parameters among animals, we predicted the circulatory equilibrium in response to changes in stressed volume in another 12 dogs under normal and heart failure conditions. This was achieved by equating the standard surface with the individually measured cardiac output (CO) curve. In this way, we could predict CO [y = 0.90x + 5.6, r(2) = 0.95, standard error of the estimate (SEE) = 8.7 ml.min(-1).kg(-1)], P(RA) (y = 0.96x, r(2) = 0.98, SEE = 0.2 mmHg), and P(LA) (y = 0.89x + 0.5, r(2) = 0.98, SEE = 0.8 mmHg) reasonably well. We conclude that the venous return surface accurately represents the venous return properties of the systemic and pulmonary circulations. The characteristics of the venous return surface are invariable enough among animals, making it possible to predict circulatory equilibrium, even if those characteristics are unknown in individual animals.

Animals↗

PubMed2001

Flow pattern of the superior caval vein in children after closure of atrial septal defect: a comparison of catheter therapy with open-heart surgery.

To compare the flow pattern of the superior caval vein (superior vena cava; SVC) after catheter therapy with that after open-heart surgery, we examined the flow velocity curves of the SVC in 10 pediatric patients who underwent catheter closure of atrial septal defect (ASD) and in 20 pediatric patients who underwent open-heart surgery. We used pulsed Doppler examinations to record the velocity curves. On the velocity curve of the SVC in children after open-heart surgery, the velocity in systole was lower than that in diastole, which is contrary to the normal pattern. The velocity in systole increased more than that in diastole during inspiration, which also differs from the normal pattern. In contrast, the velocity curve of the SVC in patients after catheter therapy showed a normal pattern. The change of flow velocity during respiration became smaller after treatment in the surgery group, although it did not change after treatment in the catheter group. These results might indicate less reserve ability in the right atrium in patients who undergo open-heart surgery. ASD closure by catheter is useful not only for its economy and noninvasiveness but also for its potential to contribute conservation of right atrial function.

Blood Flow Velocity↗

PubMed1991

Superior vena cava flow and tricuspid anular motion after cardioversion of atrial fibrillation, and role of right atrial relaxation on systolic venous return.

To determine whether atrial relaxation or systolic descent of the tricuspid anulus is the predominant factor determining systolic venous return, 22 patients with atrial fibrillation were studied. Venous return (i.e., superior vena cava (SVC) flow) was measured using pulsed Doppler echocardiography. Systolic descent of the tricuspid anulus (i.e., total excursion of tricuspid anulus during systole) was also measured using echocardiography. Serial examinations were performed before and after cardioversion of atrial fibrillation in 15 patients. In 11 patients, both the total excursion of the tricuspid anulus and SVC flow were examined in relation to the ratio of the preceding to the pre-preceding RR interval (R2/R1). Systolic forward flow of SVC increased as the ratio of late diastolic to total excursion of the tricuspid anulus (i.e., right atrial systolic function) increased. It correlated significantly with the ratio of late diastolic to total excursion of the tricuspid anulus but not with total excursion. Total excursion of the tricuspid anulus correlated significantly with R2/R1, but systolic forward flow of SVC did not. These results indicate that atrial relaxation rather than systolic descent of the tricuspid anulus was the predominant factor determining systolic forward flow in the SVC.

Atrial Fibrillation↗

PubMed1993

The influence of reproductive hormones on ANF release by rat atria.

The effects of subcutaneous (sc) administration of estradiol (50 micrograms/100 microliters/day x 10 day) or testosterone (15 mg/100 microliters twice a week x 2 weeks) on ANF release were examined in isolated perfused rat atria. The concentration of ANF in the perfusate was measured by radioimmunoassay, under basal conditions (atrial wall unstressed), and during atrial distention (intraluminal pressure raised to 4, 6, and 10 cm water). In both male and female control (vehicle-injected) groups, increased atrial pressure resulting in distention of the atrium caused a significant increase in ANF release. Estradiol increased basal secretion of ANF but did not influence stretch-induced stimulation of ANF secretion. By contrast, although testosterone did not affect basal secretion, it completely abolished the stretch-induced increase in ANF secretion. Neither estradiol nor testosterone affected atrial compliance.

Animals↗

PubMed2005

Extraction of buried P waves from printed electrocardiograms.

BACKGROUND: Morphologic identification of ectopic P-waves from surface ECGs can be challenging, particularly when the P-wave is buried in the QRST wave complex. Because ECGs are often available on paper and not digitally, we developed a method of subtracting the T-wave from the buried P-wave complex on paper ECGs. METHODS: To validate our system, an atrial extrastimulus was introduced during and following the T-wave. The ECGs were scanned and then transformed from an image format to a digital format. A computer algorithm digitally subtracted a QRST with no buried P-wave from one with a buried P-wave, thus resulting in an extracted P-wave. The extracted P-waves were compared to the nonburied P-wave by determining correlation coefficients and by visual grading by two independent reviewers. RESULTS: Visual grading comparing the buried P-wave with the exposed paced P-wave was 94%. The median correlation coefficient was 85%. CONCLUSIONS: An ectopic atrial P-wave obscured by a coincident QRST wave complex can be accurately derived from printed ECG using this PC-based system. Addition of this technique to the existing methods may aid in the localization and ablation of ectopic atrial foci.

Algorithms↗

PubMed1996

Atrial natriuretic peptide and sodium homeostasis in compensated heart failure.

The purpose of this study was to determine whether high plasma levels of atrial natriuretic peptide (ANP) in compensated heart failure are important in the maintenance of sodium balance. This was achieved by subjecting eight dogs to bilateral atrial appendectomy (APX) to blunt the ANP response to pacing-induced heart failure. Five intact dogs served as controls. In controls, 14 days of left ventricular pacing at 240 beats/min produced a sustained fall in cardiac output and mean arterial pressure of approximately 40 and 20%, respectively; compared with cardiac output, reductions in renal blood flow (up to approximately 25%) were less pronounced and even smaller decrements in GFR occurred (up to 9%). Despite these changes and a threefold elevation in plasma norepinephrine concentration, plasma renin activity (PRA) did not increase and sodium balance was achieved during the second week of pacing in association with a six- to eightfold rise in plasma levels of ANP. Similar responses occurred in four dogs in which APX was relatively ineffective in blunting the ANP response to pacing. In marked contrast, there were substantial increments in PRA and in plasma norepinephrine concentration, and marked sodium and water retention during the last week of pacing in four dogs with APX and severely deficient ANP. These results indicate that ANP plays a critical role in promoting sodium excretion in the early stages of cardiac dysfunction.

Adaptation, Physiological↗

PubMed1992

Preexisting cardiopulmonary disease attenuating the atrial natriuretic peptide response. Results in patients with acute respiratory failure.

The purpose of this study was to evaluate the pathophysiologic role of atrial natriuretic peptide (ANP) as a pulmonary artery vasodilator in patients with acute respiratory failure receiving artificial ventilation. Twenty-one consecutive patients were studied, 12 without and 9 with preexisting cardiopulmonary disease. Pulmonary artery plasma ANP levels were significantly higher than the levels obtained in the superior vena cava and radial artery. Plasma ANP levels correlated significantly with the plasma levels of its second messenger, guanosine 3',5'-cyclic monophosphate (cGMP). In the 12 patients without prior cardiopulmonary disease, plasma ANP levels correlated significantly with mean pulmonary arterial pressure (MPAP). This correlation was not found in the nine patients with preexisting cardiopulmonary disease. The cGMP/ANP ratio, indicating the biologic effect of ANP, was also higher in the patients without preexisting cardiopulmonary disease. These results are compatible with clearance and vasodilator activity of ANP in the pulmonary vascular bed, but only in patients without preexisting cardiopulmonary disease.

Acute Disease↗